A limited study was presented at a conference in Berlin, suggesting opioid release differs in problem gamblers from the general population, but in a very different way from alcoholics or other substance abusers. [26] The findings in one review indicated the sensitization theory is responsible. [27] Dopamine dysregulation syndrome has been observed in the aforementioned theory in people with regard to such activities as gambling. [28] Some medical authors suggest that the biomedical model of problem gambling may be unhelpful because it focuses only on individuals. ... The New Zealand Department of Internal Affairs. p. 28. Archived from the original (PDF) on March 21, 2012 . ... Archived from the original on November 28, 2009. CS1 maint: unfit URL ( link ) ^ Pengespill og Pengespillproblem i Norge 2007 (Report).
Description Pathologic gambling is defined as a chronic and progressive failure to resist impulses to gamble accompanied by gambling behavior that compromises or damages personal, family, or vocational pursuits. The prevalence of pathologic gambling in the adult American population is estimated to be between 1 and 3% (review by Eisen et al., 1998). Comings et al. (2001) noted that some form of gambling is legal in all but 2 states in the U.S., and gambling on the Internet is available to anyone with a computer regardless of the local laws. They stated that as access to gambling has increased, there has been a corresponding increase in the frequency of addiction to gambling, known as pathologic gambling. Inheritance Eisen et al. (1997, 1998) studied 3,359 mono- and dizygotic U.S. male twin pairs who had served in the military and found that inherited factors explained between 37 and 55% of the prevalence of 5 individual symptoms of pathologic gambling (attempts to wind back losses at same place, gambling larger amounts than intended, repeated efforts to reduce or stop gambling, frequent preoccupation with gambling, and increase betting to maintain interest) from DSM-III-R for which data was informative.
Overview Compulsive gambling, also called gambling disorder, is the uncontrollable urge to keep gambling despite the toll it takes on your life. Gambling means that you're willing to risk something you value in the hope of getting something of even greater value. Gambling can stimulate the brain's reward system much like drugs or alcohol can, leading to addiction. If you have a problem with compulsive gambling, you may continually chase bets that lead to losses, use up savings and create debt. You may hide your behavior and even turn to theft or fraud to support your addiction.
Charles Allen Moser, a physician and advocate for sexual minorities, has argued that the diagnoses should be eliminated from diagnostic manuals. [28] Typical versus atypical interests [ edit ] Albert Eulenburg (1914) noted a commonality across the paraphilias, using the terminology of his time, "All the forms of sexual perversion...have one thing in common: their roots reach down into the matrix of natural and normal sex life; there they are somehow closely connected with the feelings and expressions of our physiological erotism.
These improvements reduce the risk of cerebral contusions by providing more padding around the skull and a chin strap that keeps the helmet snug. [28] In baseball, major improvements to helmets have been made to protect batters from the impact a baseball can have when hitting their head. [29] Helmets, before this major improvement, were designed to withstand a velocity of 70 mph from a pitch or foul ball.
The decisive evidences for MEB are: MEB WWS FCMD Epidemiology [17] Finland Worldwide Japan Characteristic result of physical examination Ocular abnormalities [28] Progressive myopia with retinal degeneration Severe malformations Simple myopia and cataract without structural change Common contractures location [17] Elbow and knee Elbow Elbow, knee, ankle and hip Characteristic result of genetic test Major defected gene contributor [17] POMGNT1 POMT1, POMT2 FKTN Minor defected gene contributor [29] [30] [31] FKRP, FKTN FKRP, FCMD, LARGE, ISPD -- Characteristic result of MRI Cerebral cortex [32] Diffused dysplasia Diffused cobblestone lissencephaly Frontal polymicrogyria White matter [32] Uneven T1 and T2 prolongation No myelin in cerebrum or cerebellum Delayed cerebral myelination Others Serum creatine kinase level [8] [33] [34] Normal to elevated Elevated to high level Elevated MEB: muscle–eye–brain disease WWS: Walker–Warburg syndrome FCMD: Fukuyama congenital muscular dystrophy Management [ edit ] There is no current curative treatment for any form of muscle dystrophies and only symptomatic care is available for the patients. [17] The corresponding supportive care to symptoms is: [33] [34] Symptom Corresponding support treatment Contractures Physiological therapy and tendon-release surgery if needed Scoliosis Bracing, splinting and corrective surgery such as spinal fixation Muscle weakness Leg braces, wheelchair, occupation therapy Respiratory problem Regular monitoring by spirometry, noninvasive nighttime ventilation, tracheostomy, assisted coughing techniques Learning disabilities Specialized education programs Seizures Anti-seizures medication [35] [ better source needed ] Vision problems Wear special eye glasses [7] [35] Nutritional care Nasogastric tubes for short-term usage, gastrostomy for chronic need Prognosis [ edit ] MEB is a milder type of congenital muscle dystrophies, with a survival up to more than 70 years being possible. [34] The severity of MEB determines its prognosis.
Muscle eye brain disease (MEB) belongs to a group of genetic, degenerative muscular disorders that are present from birth ( congenital muscular dystrophy ). Individuals with this condition are born with muscle weakness (hypotonia), severe nearsightedness ( myopia ), glaucoma, and brain abnormalities. They also have developmental delay and intellectual disability, a buildup of fluid in the brain (hydrocephalus), and distinctive facial features. This condition is caused by mutations in the POMGNT1 gene and is inherited in an autosomal recessive manner. Although there is no specific treatment or cure for MEB, there are ways to manage the symptoms.
A number sign (#) is used with this entry because of evidence that this form of congenital muscular dystrophy-dystroglycanopathy with brain and eye anomalies (type A14; MDDGA14) is caused by compound heterozygous mutation in the GMPPB (615320) on chromosome 3p21. GMPPB encodes the beta subunit of GDP-mannose pyrophosphorylase. Mutation in the GMPPB gene can also cause a less severe congenital muscular dystrophy-dystroglycanopathy with mental retardation (type B14; MDDGB14; 615351) and a limb-girdle muscular dystrophy-dystroglycanopathy (type C14; MDDGC14; 615352). For a general phenotypic description and a discussion of genetic heterogeneity of muscular dystrophy-dystroglycanopathy type A, see MDDGA1 (236670). Clinical Features Carss et al. (2013) reported an 8-year-old Pakistani boy who presented at birth with increased muscle tone, microcephaly, cleft palate, and feeding difficulties. He later showed severe muscle weakness, delayed walking (only with support at age 3 years), and severe intellectual development with lack of speech.
A rare, congenital muscular dystrophy due to dystroglycanopathy characterized by early onset muscular dystrophy, severe muscular hypotonia, severe mental retardation and typical brain and eye malformations, including pachygyria, polymicrogyria, agyria, brainstem and cerebellar structural anomalies, severe myopia, glaucoma, optic nerve and retinal hypoplasia. Patients may present with seizures, macrocephaly or microcephaly, microphthalmia, and congenital contractures. Depending on the severity, limited motor function is acquired. Less severe cases have been reported.
Infants can remember the actions of sequences, the objects used to produce them, and the order in which the actions unfold, suggesting that they possess the precursors necessary for autobiographical memory . [10] Children's recall is 50% accurate for events that happened before the age of two [4] whereas adults remember near to nothing before that age. [3] By age two, children can retrieve memories after several weeks, indicating that these memories could become relatively enduring and could explain why some people have memories from this young. [3] [10] Children also show an ability to nonverbally recall events that occurred before they had the vocabulary to describe them, whereas adults do not. [18] [28] [29] Findings such as these prompted research into when and why people lose these previously accessible memories. ... Some research suggests this awareness is thought to form around the age of 4 or 5, as children in this time period can understand that recent past events affect the present, while 3-year-old children still seem unable to grasp this concept. [61] This acknowledged link of the past to the present and the concept of continuous-time and therefore a continuous self is also helped by memory talk with adults. [1] Through elaboration and repetition of events experienced, adults help children to encode memories as a part of their personal past and it becomes essential to their being. [1] Language [ edit ] The incomplete development of language in young children is thought to be a critical cause of childhood amnesia as infants do not yet have the language capacity necessary to encode autobiographical memories. [1] The typical schedule of language development seems to support this theory . [47] There appears to be a direct correlation between the development of language in children, and the earliest age at which they can obtain childhood memories (around the age 3-4). [47] Performance on both verbal and nonverbal memory tasks shows that children with more advanced language abilities can report more during a verbal interview and exhibit superior nonverbal memory compared to children with less advanced language skills. [28] If children lack language, they are unable to describe memories from infancy because they do not have the words and knowledge to explain them. ... "Adults' earliest memories as a function of age, gender, and education in a large stratified sample" (PDF) . Psychology and Aging . 28 (3): 646–653. doi : 10.1037/a0031356 . ... "Adult neurogenesis in the mammalian central nervous system". Annual Review of Neuroscience . 28 : 223–250. doi : 10.1146/annurev.neuro.28.051804.101459 . ... Recovery of “lost” infant memories in mice. Current Biology, 28(14), 2283-2290. https://doi.org/10.1016/j.cub.2018.05.059 ^ Farooq, U.; Dragoi, G. (2019-01-11).
The main lobes that are involved in decision making and complex thought processes are undergoing their final development phase during adolescence and binge drinking can negatively stunt the growth of these frontal lobes. [28] Adolescence and young adulthood [ edit ] A young man lying comatose after a binge drinking session The high levels of binge drinking among young people and the adverse consequences that include increased risk of alcoholism as an adult and liver disease make binge drinking a major public health issue. [2] Recent research has found that young college binge drinkers who drink four or more drinks on more than three occasions in the past two weeks are statistically 19 times more likely to develop alcoholism than non-binge drinkers, though the direction of causality remains unclear. [29] This is particularly interesting as drinking for the sole purpose of getting drunk, remains a major health and social problem on college campuses across the United States. [30] Heavy and regular binge drinking during adolescence is associated with an increased risk of alcoholism. ... "College binge drinking: a new approach". Journal of Consumer Marketing . 28 (3): 225–233. doi : 10.1108/07363761111127644 . ^ Charles, Janice; Valenti, Lisa; Miller, Greame (August 2011). ... I don't like Mondays. Australian Educator , 48 (1), 28-31. Retrieved from http://search.informit.com.au.ipacez.nd.edu.au/fullText;dn=146966;res=AEIPT ^ Schwandt, M.L.; S.G.
The expanded polyglutamine region results in increased affinity of the ataxin 1 AXH domain for certain transcription factors, and this effect is believed to play a significant role in ataxin 1 toxicity. [28] Another protein shown to have significant interactions with ataxin 1 is the leucine-rich acidic nuclear protein or LANP. ... HUGO gene nomenclature committee . Retrieved 28 August 2017 . ^ Zühlke C, Dalski A, Hellenbroich Y, Bubel S, Schwinger E, Bürk K (2002).
Summary Clinical characteristics. Spinocerebellar ataxia type 1 (SCA1) is characterized by progressive cerebellar ataxia, dysarthria, and eventual deterioration of bulbar functions. Early in the disease, affected individuals may have gait disturbance, slurred speech, difficulty with balance, brisk deep tendon reflexes, hypermetric saccades, nystagmus, and mild dysphagia. Later signs include slowing of saccadic velocity, development of up-gaze palsy, dysmetria, dysdiadochokinesia, and hypotonia. In advanced stages, muscle atrophy, decreased deep tendon reflexes, loss of proprioception, cognitive impairment (e.g., frontal executive dysfunction, impaired verbal memory), chorea, dystonia, and bulbar dysfunction are seen. Onset is typically in the third or fourth decade, although childhood onset and late-adult onset have been reported.
Spinocerebellar ataxia type 1 (SCA1) is a subtype of type I autosomal dominant cerebellar ataxia (ADCA type I; see this term) characterized by dysarthria, writing difficulties, limb ataxia, and commonly nystagmus and saccadic abnormalities. Epidemiology Prevalence is estimated to be 1-2 in 100,000 with significant geographical and ethnic variations. Clinical description The disease typically presents in the 4th decade (age range = 4-74 years). Ataxia gradually progresses and additional features may emerge including proprioceptive loss, hypoactive reflexes, ophthalmoparesis, and mild optic neuropathy. Initial presentation with blepharospasm, oromandibular dystonia, and retrocollis preceding ataxia has been reported.
Spinocerebellar ataxia type 1 (SCA1) is a condition characterized by progressive problems with movement. People with this condition initially experience problems with coordination and balance (ataxia). Other signs and symptoms of SCA1 include speech and swallowing difficulties, muscle stiffness (spasticity), and weakness in the muscles that control eye movement (ophthalmoplegia). Eye muscle weakness leads to rapid, involuntary eye movements (nystagmus). Individuals with SCA1 may have difficulty processing, learning, and remembering information (cognitive impairment).
A number sign (#) is used with this entry because spinocerebellar ataxia-1 (SCA1) is caused by an expanded (CAG)n trinucleotide repeat in the ataxin-1 gene (ATXN1; 601556) on chromosome 6p22. Description The autosomal dominant cerebellar degenerative disorders are generally referred to as 'spinocerebellar ataxias,' (SCAs) even though 'spinocerebellar' is a hybrid term, referring to both clinical signs and neuroanatomical regions (Margolis, 2003). Neuropathologists have defined SCAs as cerebellar ataxias with variable involvement of the brainstem and spinal cord, and the clinical features of the disorders are caused by degeneration of the cerebellum and its afferent and efferent connections, which involve the brainstem and spinal cord (Schols et al., 2004; Taroni and DiDonato, 2004). Historically, Harding (1982) proposed a clinical classification for autosomal dominant cerebellar ataxias (ADCAs). ADCA I was characterized by cerebellar ataxia in combination with various associated neurologic features, such as ophthalmoplegia, pyramidal and extrapyramidal signs, peripheral neuropathy, and dementia, among others.
Spinocerebellar ataxia type 1 (SCA1) is a progressive movement disorder that typically begins in early adulthood (but can affect children and older adults as well). Early signs and symptoms includes problems with coordination and balance (ataxia), speech and swallowing difficulties, muscle stiffness, and weakness in the muscles that control eye movement. Over time, SCA1 may cause mental impairment, numbness, tingling, or pain in the arms and legs and uncontrolled muscle tensing, wasting, and twitches. SCA1 is caused by changes in the ATXN1 gene and is inherited in an autosomal dominant fashion. There is currently not a cure for SCA1, but treatments are available to help manage symptoms.
Recent review studies suggest that the IGDS9-SF presents with robust empirical and clinical evidence and is an effective tool to assess IGD. [24] [25] Moreover, the scale was adapted in several languages as Spanish, [26] [27] [28] Chinese, [29] Czech, [30] German, [31] and so many more. ... After previously having spent two straight days playing online role-playing games in an Internet cafe, Zhang had told his parents that he had "been poisoned by games and could no longer control himself". [127] The head of a software association said to gaming website Play.tm that same year: "In the hypothetical world created by such games, [players] become confident and gain satisfaction, which they cannot get in the real world." [127] In 2007, a 26-year-old man identified only as "Zhang" died of a heart attack due to lack of physical activity following a seven-day gaming binge, [128] while a 30-year-old man died in a Guangzhou Internet cafe after playing online games for three straight days. [129] [130] South Korea [ edit ] In 2005, 28-year old industrial repairman Seungseob Lee ( Hangul : 이승섭) visited an Internet cafe in the city of Daegu and played StarCraft almost continuously for fifty hours. ... Engadget . Archived from the original on 28 December 2017 . Retrieved 27 December 2017 . ^ a b c Pontes HM, Schivinski B, Sindermann C, Li M, Becker B, Zhou M, Montag C (June 2019).
The person may also be punished by a fine not to exceed $1,000.00 and/or by imprisonment in the common jail of the town not to exceed six months. [27] The Animal Law Coalition has a Model Animal Hoarding Specific Ordinance (available under “Resources” at its website) that can be adapted by various communities. [28] More controversially, a municipality may limit the number of pets a person is allowed to keep in his or her home in hopes of preventing animal hoarding. ... California Lawyer (September): 26, 28, 29, 67. Archived from the original (PDF) on July 3, 2004. ^ a b Hoarding of Animals Research Consortium (HARC) (2004).
In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), zoophilia is placed in the classification "other specified paraphilic disorder" [24] (" paraphilias not otherwise specified" in the DSM-III and IV [25] [26] [27] [28] ). The World Health Organization takes the same position, listing a sexual preference for animals in its ICD -10 as "other disorder of sexual preference". [29] In the DSM-5, it rises to the level of a diagnosable disorder only when accompanied by distress or interference with normal functioning. [24] [30] Zoophilia may also be covered to some degree by other fields such as ethics, philosophy, law, animal rights and animal welfare .
For example, one study found that the introduction of latrines into a resource-limited community only reduced the prevalence of hookworm infection by four percent. [27] However, another study in Salvador, Brazil found that improved drainage and sewerage had a significant impact on the prevalence of hookworm infection but no impact at all on the intensity of hookworm infection. [28] This seems to suggest that environmental control alone has a limited but incomplete effect on the transmission of hookworms. ... Archived from the original on 4 December 2014 . Retrieved 28 November 2014 . ^ James, William D.; Berger, Timothy G.; et al. (2006). ... World Bank. 2003. ^ "Soil-transmitted helminthiasis" . Wkly. Epidemiol. Rec . 83 (27/28): 237–252. 4 July 2008. ^ "How does deworming work?"
Ancylostomiasis Other names Anchylostomiasis, Ankylostomiasis Infective larva of Necator americanus Specialty Tropical medicine , infectious disease , parasitology Ancylostomiasis is a hookworm disease caused by infection with Ancylostoma hookworms . The name is derived from Greek ancylos αγκύλος "crooked, bent" and stoma στόμα "mouth". Ancylostomiasis is also known as miner's anaemia , tunnel disease , brickmaker's anaemia and Egyptian chlorosis . Helminthiasis may also refer to ancylostomiasis, but this term also refers to all other parasitic worm diseases as well. In the United Kingdom, if acquired in the context of working in a mine, the condition is eligible for Industrial Injuries Disability Benefit.
The bill was referred to the House Health and Welfare Committee on February 20, 2013; it did not advance out of the committee. [27] [28] They tried to ban abortion that year, one of five states to do so.
For instance, while trying to turn over to the next page with the right hand, his left hand would try to close the book. [27] In another case of callosal alien hand, the patient did not suffer from intermanual conflict between the hands but rather from a symptom characterized by involuntary mirror movements of the affected hand. [28] When the patient was asked to perform movements with one hand, the other hand would involuntarily perform a mirror image movement which continued even when the involuntary movement was brought to the attention of the patient, and the patient was asked to restrain the mirrored movement. ... In both of these variants of alien hand syndrome, the alien hand emerges in the hand contralateral to the damaged hemisphere. [ citation needed ] Treatment [ edit ] There is no cure for the alien hand syndrome. [28] However, the symptoms can be reduced and managed to some degree by keeping the alien hand occupied and involved in a task, for example by giving it an object to hold in its grasp.
Comorbidity [ edit ] Externalizing disorders are frequently comorbid or co-occurring with other disorders. [13] [14] Individuals who have the co-occurrence of more than one externalizing disorder have homotypic comorbidity, whereas individuals who have co-occurring externalizing and internalizing disorders have heterotypic comorbidity. [15] It is not uncommon for children with early externalizing problems to develop both internalizing and further externalizing problems across the lifespan. [15] [16] [17] Additionally, the complex interplay between externalizing and internalizing symptoms across development could explain the association between these problems and other risk behaviors, that typically initiate in adolescence (such as antisocial behaviors and substance use). [18] Stigma [ edit ] Consistent with many mental disorders, [19] individuals with externalizing disorders are subject to significant implicit and explicit forms of stigma. [20] Because externalizing behaviors are salient and difficult to conceal, individuals with externalizing disorders may be more susceptible to stigmatization relative to individuals with other disorders. [21] Parents of youth with childhood mental disorders, such as ADHD and ODD, are frequently stigmatized when parenting practices are strongly implicated in the etiology or cause of the disorder. [21] Educational and policy-related initiatives have been proposed as potential mechanisms to reduce stigmatization of mental disorders. [22] Psychopathic traits [ edit ] Individuals with psychopathic traits , including callous-unemotional (CU) traits , represent a phenomenologically and etiologically distinct group with severe externalizing problems. [23] Psychopathic traits have been measured in children as young as two-years-old, [23] are moderately stable, [23] [24] are heritable, [24] and associated with atypical affective, [23] [24] cognitive, personality, and social characteristics. [23] Individuals with psychopathic traits are at risk for poor response to treatment, [25] however, some data suggest that parent management training interventions for youth with psychopathic traits early in development may have promise. [23] [24] [25] Developmental course [ edit ] ADHD often precedes the onset of ODD, and approximately half of children with ADHD, combined type also have ODD. [10] ODD is a risk factor for CD and frequently precedes the onset of CD symptoms. [26] Children with an early onset of CD symptoms, with at least one symptom before age 10 years, [2] are at risk for more severe and persistent antisocial behavior continuing into adulthood. [26] [27] Youth with early-onset conduct problems are particularly at risk for ASPD (note that an onset of CD prior to age 15 is part of the diagnostic criteria for ASPD), [2] whereas CD is typically limited to adolescence when youth's CD symptoms begin during adolescence. [26] Treatment [ edit ] Despite recent initiatives to study psychopathology along dimensions of behavior and neurobiological indices, which would help refine a clearer picture of the development and treatment of externalizing disorders, the majority of research has examined specific mental disorders. [28] Thus, best practices for many externalizing disorders are disorder-specific.
Protection by HbAS involves the enhancement of not only innate but also of acquired immunity to the parasite. [24] Prematurely denatured sickle hemoglobin results in an upregulation of natural antibodies which control erythrocyte adhesion in both malaria and sickle cell disease. [25] Targeting the stimuli that lead to endothelial activation will constitute a promising therapeutic strategy to inhibit sickle red cell adhesion and vaso-occlusion. [26] This has led to the hypothesis that while homozygotes for the sickle cell gene suffer from disease, heterozygotes might be protected against malaria. [27] Malaria remains a selective factor for the sickle cell trait. [28] Thalassemias [ edit ] Main articles: Thalassemia and Alpha-thalassemia It has long been known that a kind of anemia, termed thalassemia , has a high frequency in some Mediterranean populations, including Greeks and southern Italians. ... Archived from the original (PDF) on 2011-09-28. ^ a b Miller LH, Mason SJ, Clyde DF, McGinniss MH (1976).
Although mild, flu-like symptoms occasionally occur during the first few weeks following exposure, infection with T. gondii produces no readily observable symptoms in healthy human adults. [7] [19] In most immunocompetent people, the infection enters a latent phase, during which only bradyzoites ( in tissue cysts ) are present; [20] these tissue cysts and even lesions can occur in the retinas , alveolar lining of the lungs (where an acute infection may mimic a Pneumocystis jirovecii infection), heart, skeletal muscle, and the central nervous system (CNS), including the brain. [21] Cysts form in the CNS ( brain tissue ) upon infection with T. gondii and persist for the lifetime of the host. [22] Most infants who are infected while in the womb have no symptoms at birth, but may develop symptoms later in life. [23] Reviews of serological studies have estimated that 30–50% of the global population has been exposed to and may be chronically infected with latent toxoplasmosis, although infection rates differ significantly from country to country. [7] [24] [25] This latent state of infection has recently been associated with numerous disease burdens , [7] neural alterations, [22] [24] and subtle gender-dependent [ dubious – discuss ] behavioral changes in immunocompetent humans, [26] [27] as well as a increased risk of motor vehicle collisions. [28] Skin [ edit ] While rare, skin lesions may occur in the acquired form of the disease, including roseola and erythema multiforme-like eruptions, prurigo -like nodules, urticaria , and maculopapular lesions .
Overview Toxoplasmosis (tok-so-plaz-MOE-sis) is an infection with a parasite called Toxoplasma gondii. People often get the infection from eating undercooked meat. You can also get it from contact with cat feces. The parasite can pass to a baby during pregnancy. Most people infected with the parasite do not have symptoms. Some people get flu-like symptoms. Serious disease most often affects infants and people with weakened immune systems. Toxoplasmosis during pregnancy may cause miscarriage and birth defects.
Speech sound disorder (SSD) is any problem with speech production arising from any cause. [26] Speech sound disorders of unknown cause that are not accompanied by other language problems are a relatively common reason for young children to be referred to speech-language therapy (speech-language pathology). [27] These often resolve by around 4–5 years of age with specialist intervention, [28] and so would not meet criteria for DLD.
Drug treatment programs in Europe often report more favorable outcomes than those in the US because the criteria for measuring success are functional rather than abstinence-based. [25] [26] [27] The supporters of programs with total abstinence from drugs as a goal believe that enabling further drug use means prolonged drug use and risks an increase in addiction and complications from addiction. [28] Residential [ edit ] Residential drug treatment can be broadly divided into two camps: 12-step programs and therapeutic communities. 12-step programs are a nonclinical support-group and spiritual-based approach to treating addiction. ... In the past decade, there have been growing efforts through state and local legislations to shift from criminalizing drug abuse to treating it as a health condition requiring medical intervention. 28 states currently allow for the establishment of needle exchanges. ... Retrieved 12 June 2015 . ^ "Diagnostic and Statistical Manual of Mental Disorders: DSM-5 (5th edition)2014 102 Diagnostic and Statistical Manual of Mental Disorders: DSM-5 (5th edition) Washington, DC American Psychiatric Association 2013 xliv+947 pp. 9780890425541(hbck);9780890425558(pbck) £175 $199 (hbck); £45 $69 (pbck)". Reference Reviews . 28 (3): 36–37. 11 March 2014. doi : 10.1108/rr-10-2013-0256 . ... Archived from the original on 11 November 2017 . Retrieved 28 April 2018 . ^ Nutt D, King LA, Saulsbury W, Blakemore C (March 2007). ... S2CID 27080462 . ^ "Drug Addicts Anonymous UK" . www.drugaddictsanonymous.org.uk . Archived from the original on 28 December 2017 . Retrieved 28 April 2018 . ^ "Preventing Drug Relapse: What Are the Steps?
As a result of this unclear classification, flukes in Japan are normally referred to as Fasciola spp. [28] Recent reports based on mitochondrial genes analysis has shown that Japanese Fasciola spp. is more closely related to F. gigantica than to F. hepatica . [29] In India, a species called F. jacksoni was described in elephants . [30] Transmission [ edit ] Human F. hepatica infection is determined by the presence of the intermediate snail hosts, domestic herbivorous animals, climatic conditions and the dietary habits of man. [31] Sheep, goats and cattle are considered the predominant animal reservoirs . ... ISBN 9780702053061 . ^ "Neglected Tropical Diseases" . cdc.gov . June 6, 2011 . Retrieved 28 November 2014 . ^ a b "CDC - Fasciola - Treatment" . www.cdc.gov . ... "Chronic subclinical ovine fascioliasis: plasma glutamate dehydrogenase, gamma glutamyl transpeptidase and aspartate aminotransferase activities and their significance as diagnostic aids". Res. Vet. Sci . 28 (1): 71–78. doi : 10.1016/S0034-5288(18)32775-9 . ... "Triploid form of Fasciola in Japan: genetic relationships between Fasciola hepatica and Fasciola gigantica determined by ITS-2 sequence of nuclear rDNA". Int. J. Parasitol . 28 (5): 777–81. doi : 10.1016/S0020-7519(98)00037-X .
Emotional factors include interpersonal or psychological problems, which can be the result of depression , sexual fears or guilt, past sexual trauma, and sexual disorders, [28] among others. Sexual dysfunction is especially common among people who have anxiety disorders . ... The Medical Clinics of North America . 99 (3): 607–28. doi : 10.1016/j.mcna.2015.01.011 .